DNA strand breaks, oxidative damage, and 1-OH pyrene in roofers with coal-tar pitch dust and/or asphalt fume exposure

Objective: To determine the potential for asphalt fume exposure to increase DNA damage, we conducted a cross-sectional study of roofers involved in th e application of roofing asphalt. Methods: DNA strand breaks and the ratio of 8-hydroxydeoxyguanosine (8-OHdG) to 2-deoxyguanosine (dG) were measured in peripheral blood leukocytes of roofers. In addition, urinary excretion o f 8-OHdG and 8-epi-prostaglandin F-2 alpha (8-epi-PGF) was also measured. T he study population consisted of 26 roofers exposed to roofing asphalt and 15 construction workers not exposed to asphalt during the past 5 years. A s ubset of asphalt roofers (n = 19) was exposed to coal-tar pitch dust (coal tar) during removal of existing roofs prior to applying hot asphalt. Person al air monitoring was performed for one work-week to measure exposure to to tal particulates, benzene-soluble fraction of total particulates, and polyc yclic aromatic compounds (PACs). Urinary 1-OH-pyrene levels were measured a s an internal biomarker of PAC exposure. Results: Full-shift breathing zone measurements for total particulates, benzene-solubles and PACs were signif icantly higher for coal-tar exposed workers than for roofers not exposed to coal tar. Similarly, urinary I-OH-pyrene levels were higher in coal-tar ex posed roofers than roofers not exposed to coal tar. Total particulates or b enzene-soluble fractions were not associated with urinary I-OH-pyrene, but PAC exposure was highly correlated with urinary 1-OH-pyrene. When stratifie d by I-OH-pyrene excretion, DNA strand breaks increased in a dose-dependent manner, and leukocyte 8-OHdG/dG decreased in a dose-dependent manner. Sign ificant changes in DNA damage appeared to be linked to PACs from coal-tar e xposure, although asphalt fume alone was associated with a small but signif icant increase in urinary 1-OH-pyrene and DNA strand breaks. Conclusions: R esults are consistent with previous reports that asphalt or coal-tar exposu re can cause DNA damage. Urinary 8-epi-PGF remained relatively constant dur ing the week for virtually all subjects, regardless of exposure indicating that neither asphalt nor coal-tar exposure induces an overt oxidative stres s. A small, but statistically significant increase in 8OHdG was evident in end-of-week urine samples compared with start-of-week urine samples in roof ers exposed to coal-tar. The increase in urinary 8OHdG coupled with the dec rease in leukocyte 8-OHdG/dG, suggests that coal-tar exposure induces prote ctive or repair mechanisms that result in reduced levels of steady-state ox idative-DNA damage.